ArticlePLoS pathogens2014
Silencing by H-NS potentiated the evolution of Salmonella.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
66 citing papers in PubMed, 97 citations in OpenAlex.
- Perturbing H-NS function reveals roles in restricting virulence heterogeneity and pathogen adaptation.PLoS pathogens · 2026Article
- Phage-encoded sRNA counteracts xenogeneic silencing in pathogenic E. coli.PLoS pathogens · 2026Article
- Perturbing H-NS function reveals roles in restricting virulence heterogeneity and pathogen adaptation.bioRxiv : the preprint server for biology · 2026Article
- Cyclic-di-GMP interferes with DNA-MucR-DNA bridging to derepress genes targeted by the xenogeneic silencer MucR.Nucleic acids research · 2025Article
- Nucleoid-associated proteins: molecular mechanisms in microbial adaptation.World journal of microbiology & biotechnology · 2025Review
- A scalable gut epithelial organoid model reveals the genome-wide colonization landscape of a human-adapted pathogen.Nature genetics · 2025Article
- ChIP-mini: a low-input ChIP-exo protocol for elucidating DNA-binding protein dynamics in intracellular pathogens.Nucleic acids research · 2025Article
- Hierarchic regulation of a metabolic pathway: H-NS, CRP, and SsrB controlMicrobiology spectrum · 2024Article
- c-di-GMP inhibits the DNA binding activity of H-NS in Salmonella.Nature communications · 2023Article
- VirB, a key transcriptional regulator ofmBio · 2023Article
- Advancing evolution: Bacteria break down gene silencer to express horizontally acquired genes.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Article
- VirB, a key transcriptional regulator ofbioRxiv : the preprint server for biology · 2023Article
- Localized modulation of DNA supercoiling, triggered by the Shigella anti-silencer VirB, is sufficient to relieve H-NS-mediated silencing.Nucleic acids research · 2023Article
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- Pervasive transcription enhances the accessibility of H-NS-silenced promoters and generates bistability inProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Regulatory Evolution of theJournal of bacteriology · 2022Article
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- Long-Distance Effects of H-NS Binding in the Control ofJournal of bacteriology · 2021Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The bacterial H-NS protein silences expression from sequences with higher AT-content than the host genome and is believed to buffer the fitness consequences associated with foreign gene acquisition. Loss of H-NS results in severe growth defects in Salmonella, but the underlying reasons were unclear. An experimental evolution approach was employed to determine which secondary mutations could compensate for the loss of H-NS in Salmonella. Six independently derived S. Typhimurium hns mutant strains were serially passaged for 300 generations prior to whole genome sequencing. Growth rates of all lineages dramatically improved during the course of the experiment. Each of the hns mutant lineages acquired missense mutations in the gene encoding the H-NS paralog StpA encoding a poorly understood H-NS paralog, while 5 of the mutant lineages acquired deletions in the genes encoding the Salmonella Pathogenicity Island-1 (SPI-1) Type 3 secretion system critical to invoke inflammation. We further demonstrate that SPI-1 misregulation is a primary contributor to the decreased fitness in Salmonella hns mutants. Three of the lineages acquired additional loss of function mutations in the PhoPQ virulence regulatory system. Similarly passaged wild type Salmonella lineages did not acquire these mutations. The stpA missense mutations arose in the oligomerization domain and generated proteins that could compensate for the loss of H-NS to varying degrees. StpA variants most able to functionally substitute for H-NS displayed altered DNA binding and oligomerization properties that resembled those of H-NS. These findings indicate that H-NS was central to the evolution of the Salmonellae by buffering the negative fitness consequences caused by the secretion system that is the defining characteristic of the species.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.